Evidence map›Paper›PMID 12947395›Full record

ReviewOncogene2003

MAPK pathways in radiation responses.

Paul Dent, Adly Yacoub, Paul B Fisher, Michael P Hagan, Steven Grant

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 258 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
258citing papers in PubMed, 1 pooled it
30.6field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

258 citing papers in PubMed, 1 synthesis or guideline pooled it, 597 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Radiosensitization of Glioblastoma by the K-ras Inhibitor RMC-6236.bioRxiv : the preprint server for biology · 2026
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198 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Paul DentDepartment of Radiation Oncology, Virginia Commonwealth University, Richmond, VA 23298-0058, USA. pdent@hsc.vcu.edu
Adly Yacoub
Paul B Fisher
Michael P Hagan
Steven Grant
Virginia Commonwealth University · USColumbia University · US

Funding

RADIOSENSITIZATION OF MALIGNANT GLIOMAS BY VIRAL TRANSDUCTION WITH WILD-TYPE P53P01CA072955 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI VALERIE, KRISTOFFER CARL · 1998 to 2007
$6.0M
Carcinoma cell radiosensitization by MAPK inhibitionR01CA088906 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI DENT, PAUL · 2001 to 2004
$783k
NCI NIH HHS CA72955NCI NIH HHS CA88906NIDDK NIH HHS DK52875
6 · The paper itself

Abstract

Within the last 15 years, multiple new signal transduction pathways within cells have been discovered. Many of these pathways belong to what is now termed 'the mitogen-activated protein kinase (MAPK) superfamily.' These pathways have been linked to the growth factor-mediated regulation of diverse cellular events such as proliferation, senescence, differentiation and apoptosis. Based on currently available data, exposure of cells to ionizing radiation and a variety of other toxic stresses induces simultaneous compensatory activation of multiple MAPK pathways. These signals play critical roles in controlling cell survival and repopulation effects following irradiation, in a cell-type-dependent manner. Some of the signaling pathways activated following radiation exposure are those normally activated by mitogens, such as the 'classical' MAPK (also known as the ERK) pathway. Other MAPK pathways activated by radiation include those downstream of death receptors and procaspases, and DNA-damage signals, including the JNK and P38 MAPK pathways. The expression and release of autocrine growth factor ligands, such as (transforming growth factor alpha) and TNF-alpha, following irradiation can also enhance the responses of MAPK pathways in cells and, consequently, of bystander cells. Thus, the ability of radiation to activate MAPK signaling pathways may depend on the expression of multiple growth factor receptors, autocrine factors and Ras mutation. Enhanced basal signaling by proto-oncogenes such as K-/H-/N-RAS may provide a radioprotective and growth-promoting signal. In many cell types, this may be via the PI3K pathway; in others, this may occur through nuclear factor-kappa B or multiple MAPK pathways. This review will describe the enzymes within the known MAPK signaling pathways and discuss their activation and roles in cellular radiation responses.

Indexed as

AnimalsCell SurvivalHumansJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase 5Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesSignal TransductionJNK Mitogen-Activated Protein KinasesMAP2K5 protein, humanMAP Kinase Kinase 5Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-Kinases

Identifiers

PMID12947395
OpenAlexW2049048127

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.